Pharm Exam II Flashcards
Hypertension
Prevalent and common chronic disorder that affects 50-60 million adults. Can be very dangerous. If left untreated, you can have a greater risk for CHF, cardiac infarction, cerebral infarction. Kidney failure due to high blood pressure running through the sensitive tissue.
Angiogram
put dye through someone’s bloodvessels to see if there is blockage in the heart
Function of Cardiac Cycle
Bring oxygen to the myocardium and tissues
Pulmonary Artery
only artery that carries deoxygenated blood.
2 phases of Cardiac Cycle
Systole and Diastole
Systole
contraction of the ventricles of the heart that occurs between the first and second heart sounds of the cardiac cycle
Diastole
the part of the cardiac cycle during which the heart refills with blood after the emptying done during systole. Resting state
Stroke Volume
amount of blood ejected from the left ventricle with each contraction
Preload
end-diastolic volume. Amount of blood left in the left ventricle
Afterload
resistance to left ventricular ejection: the work the heart must overcome to eject blood.
Contractility
Ability of the heart muscle to contract
Cardiac Output
amount of blood pumped by the heart each minute
Cardiac Output Equation
Heart Rate x Stroke Volume
Cardiac Conduction Pathway
SA node:AV node:BUndle of HIS:Right+Left Bundle Branches:Purkinje Fibers
SA node
pacemaker of the heart
Atrioventricular Node
Receives the message from the SA node. Has the ability to slow so that the ventricles fill properly. This is the filter
Purkinje Fibers
Causes the contraction or squeeze of the ventricles
Cardiac Blood Flow
Venous Deoxygenated return to heart
arterial oxygenated outflow to the body
Venous pressure system is lower so it needs valves
Pulse Pressure
This number represents the filling pressure of the arteries
Systolic blood pressure minus diastolic blood pressure.
Vasomotor Center
Made up of Baroreceptors and Chemoreceptors
Chemoreceptors
respond to oxygen, carbon dioxide, and pH changes, increases or decreases
Baroreceptors:
respond to increase of decrease in pressure or stretch
Anger or stress effect on BP
elevates your blood pressure
Depression or lethargy
deplete blood pressure
Antidiuretic Hormone (ADH)
released to increase blood pressure. This will keep the fluid volume in your body. It is going to NOT produce this when you are HTN because it wants you to get rid of blood volume
Renin-angiotension-aldosterone system (RAAS)
blood pressure regulation by modulating blood volume, sodium reabsorption, potassium secretion, water reabsorption, and vascular tone
Peripheral Resistance/Diameter of arterioles
how much pressure is in the arterials/lack of pressure in the venous system. This is emphasized by sympathetic nervous system activity. Activation of SNS. Has effect on BP
Viscosity
increase in blood viscosity is typically related to dehydration and will raise the blood pressure.
Lack of O2 effect on BP
increase because the body thinks that it is time to speed up for proper perfusion
Cellular metabolism by-product accumulation effect on BP
(CO2/lactic acid). Occurs when people are septic
Histamine
release dilates blood vessels/lowers BP
Bradykinin
potent peptide causing vasodilation/lowers BP
Prostaglandin
includes both vasodilators and vasoconstrictors
Arterial blood Pressure:
force exerted on arterial walls by blood flow. This is most affected by Systolic BP and Diastolic BP
Frank Starling Law
The more volume of blood in the heart during diastole, the more forceful the cardiac contraction, the more blood the ventricle will pump.
Exception: cardiomyopraphy
cardiomyopraphy
the muscles of the heart get stretched out
When the body’s blood pressure increases, two things might happen:
- Compensatory action by the cardiovascular system might occur which will cause vasodilation, decreased stroke volume, decreased heart rate (which will in turn decrease the cardiac output). All of these things will lower the blood pressure
- Compensatory action by the kidney’s: increased urine output will decrease the blood urine which will decrease the BP
Hypotension
Systolic less than 90
Response to Hypotension
SNS is stimulated.
- Adrenal medulla secretes epinephrine and norepinephrine
-Angiotensin II and aldosterone are formed
-Kidney’s retain fluid and blood pressure is increased
Response to Hypertension:
Increases renal secretion (increases urine output), fluid loss, less circulating volume, decrease in cardiac output, decrease in arterial blood pressure
Definition HTN
persistently high blood pressure (increase force in arteries) that results from abnormalities in regulatory mechanism.
Systolic pressure greater than 140mmHg
Diastolic Pressure greater than 90mmHg
PreHTN
S=120-139|D=80-90
Stage 1 HTN
130-139
Stage 2 HTN
140+
Primary HTN
90%-95% of cases: complex physiological condition where the cause is unknown.
Secondary HTN
may result from renal artery stenosis, endocrine, or CNS disorders from medications. Results from an identifiable cause. We know why they have it.
Effects of BP
MI (tires out the heart), CHF, stroke, renal disease, retinal damage
myocardial hypertrophy
muscle works hard, but it doesnt get bigger in to out. It gets bigger out to in. The walls start to thicken and it reduces the size of the ventricles which reduces perfusion
ADH: (Antidiuretic Hormone):
released in response to an increase in blood osmolality (blood gets thicker in a dehydrated state)
Promotes reabsorption of water by the kidneys to try to get the thicker blood to be thinner.
Decreases the urine output
INcrease in circulating blood volume which will in turn increase the Na+ and water in the body
Loss of K+ in urine
Potent vasoconstrictor
Synthetic vasopressin admin to treat DI and hypotensive crisis
Renin-Angiotensinogen-Aldosterone System
Liver constantly produces angiotensinogen in the plasma
Renin is produced in response to low BP which reacts with angiotensinogen to make angiotensin I
Angiotensin converting enzyme takes the angiotensin 1 and makes it angiotensin 2 which produces aldosterone (rom adrenal cortex)
This causes reabsorption of Na+ and H2O
White coat syndrome
afraid to come to the doctor’s office and their blood pressure goes up.
Non-Pharmacological Agents to help with BP:
Stress management
Limit ETOH (alcohol) (male 2 or less a day. Women 1 to less a day)
REduce sodium
Reduce fat and cholesterol
Increase fruit and vegetables
Increase aerobic physical activities
Discontinue tobacco products
Maintain optimum weight
Angiotensin Converting Enzyme Inhibitors: ACE inhibitors
Inhibit the conversion of angiotensin I to angiotensin II
-Ex. CaptoPRIL, enalaPRIL, lisinoPRIL, remiPRIL
ACE I side Effects:
ACE cough (ticky cough)
Angioedema (swelling around oral cavity that is a 911)
Hyperkalemia. Avoid K+ supplements, K sparing diuretics, or foods high in K+, or salt substitutes
Orthostatic hypotension
Peptic Ulcers, gastric irritation
Acute renal failure (kidneys regulate K+)
HA/Dizzy
When to take ACE
Take 1 hour before or 2 hours after a meal (lisinopril can be taken with food)
Black Box ACE
causes injury and death to fetus
Angiotensin II Receptor Blockers (ARBs):
Selectively bind to angiotensin II receptors in vascular smooth muscle and adrenal cortex.
Insurance wont pay for these ones upon first visit
Ex. Losartan, Valsartan, olmesartan
ARB side effects:
Orthostatic Hypotension
HA, dizziness, diarrhea
Dry Mouth
angioedema
Acute renal failure: watch BUN, Creatinine, and GFR
Hyperkalemia: blocking the angiotensin II in the cascade
ARB Dose Dependent:
once daily for HTN treatment/Twice daily for CHF monitor K+
Black Box for all ARBS
pregnancy: known to cause injury or death to the fetus
Calcium Channel Blockers:
Treatment for HTN. Inhibit the movement of Ca+ ions across the membranes of myocardial and arterial muscle cells. Decrease in HR and causes vasodilation of the peripheral vasculature
Medication that are Calcium Channel Blockers
amlodipine, diltiazem, verapamil, nicardipine, nifedipine
Ca+ blocker side effects
Flushed skin, muscle cramps, peripheral edema
HA, dizziness, hypotension
Impotence, sexual dysfunction
Hepatotoxicity (interacts with alcohol)
Angioedema
Contraindications: renal impairment, CHF/heart block, or pregnancy
Interacts with macrolide antibiotics and grapefruit juice
Antiadrenergic Medications
Inhibits the SNS=decreases HR, decreases the force of myocardial contraction, cardiac output, and blood pressure
Alpha1 Adrenergic receptor blockers:
dilate blood vessels and decrease peripheral vascular resistance (PVR)
Alpha1 Adrenergic receptor blockers Examples
doxazosin, prazosin, terazosin
Side Effects of A1 Adrenergic Blockers
first dose phenomenon:ortho-hypotn, dizziness, palpitations, syncopal episode (drops so low they pass out)
First does, increase dose (start low go slow)=given at night to prevent SE
Can have increase Na+/fluid retention
Alpha2-receptor agonists:
Inhibits norepinephrine, has an antiadrenergic effect, decreases CO, decrease HR, decreases PVR, decreases BP
Examples of Alpha2-receptor agonists:
clonidine (strong), methyldopa, guanfacine
Beta Adrenergic Blockers:
Decrease HR, force of myocardial contraction, CO and renin release from the kidneys
Beta Adrenergic Blockers Medications
atenolol, metoprolol, propranolol
When to use Beta Adrenergic Blockers:
First medication for patients under 50 with cardio selective medications. first choice in patients with asthma, PVD, or DM. Make sure you have a selective beta blocker for asthma or COPD patients
bid or hold for HR less than 60bpm
Beta Adrenergic Blockers TX
HTN, Dysrhythmias, HF, MI, and narrow angle glaucoma
Side effects of B-Andrenergic Blockers
hypotension, bradycardia, dizziness (caution in pt. With liver impairment)
Black Box for all beta adrenergic blockers
Don’t stop abruptly. For patients with CAD (coronary artery disease), dose must be titrated down prior to discontinuing. If not, RF rebound angina (chest pain), vent dysrhythmias, MI
Side effect of Beta Blocker
This medication can cause erectile dysfunction.
Alpha-Beta Adrenergic Blockers
carvedilol, labetalol.
Dual Action in one tablet
Diuretics
Reduction of blood volume through urinary excretion of H2O and electrolytes.
Often used as a first line rx in mild-mod HTN
Thiazide + Thiazide-like diuretics
block Na+ reabsorption, increase K+ and H2O secretion
Ex. hydrochlorothiazide
Potassium-sparing diuretics
spironolactone
excretion of Na+ and retention of K+
K+ sparing diuretic
Use for someone with low K.
K+ Importance
response for contractility of the heart
spironolactone
Potassium-sparing diuretics
Can increase effects of digoxin, monitor for hyperKalemia in patients also taking ACE/ARB
Loop Diuretics:
Inhibit reabsorption of Na+ and Cl- in the loop of Henle.
K+ wasting diuretic
Furosemide: always monitor K+
Can increase digoxin levels, cause hypoKalemia
Furosemide
Loop Diuretic. Can increase digoxin levels
Direct Acting Vasodilators
Directly relax smooth muscles in the blood vessels=dilation and decreased PVR
hydralazine, nitroprusside (IV only)
Ventricular Tachycardia
very rapid contraction of the ventricles. Very dangerous because the ventricles pump so hard that the heart might lead to cardiac arrest.
Asystole
straight line on an EKG.
Dysrhythmia/Arrhythmia
abnormality in a physiological rhythm; especially in the activity of the brain or heart
contractile tissue
Electricity resides in specialized tissues that generate and conduct electrical impulses
Regular intervals with four events
stimulation from electrical impulse=transmission to adjacent tissue=contraction of atria, then ventricles=relaxation of atria, then ventricles
Automaticity
ability of the heart to generate an electrical impulse
Any part of conduction system can start an impulse
Conductivity
ability of cardiac tissue to transmit the electrical impulse.
Why is the SA node the pacemaker
It has the fastest rate of automaticity (pacemaker)
Initiation of the impulse is dependent on Na and K ion movement
Absolute refractory period
Period of decreased excitability/cells cannot respond to new stimulation
P wave
measures the electrical depolarization of the atria
QRS wave
has to do with bundle branches and purkinje network
T wave
has to do with ventricular repolarization
Dysrhythmia
abnormality in cardiac rate or rhythm
Can originate in any part of the conduction system
Automaticity
allows cells other than SA node to initiate electrical impulse that reaches the highest level of contraction
SA node failure to slow depolarization
Built in defense mechanism. AV node can take over if SA node is failing
ectopic focus/ectopic beat
Impulse origination other than in SA node
Indicates myocardial irritability
Activation of ectopic focus/ectopic beat
Hypoxia (low O2 in blood), ischemia (no blood to tissue), hypokalemia (low potassium)
Tachycardia
beating faster than normal. Can occur in Ventricles or Atria.
Sinus Tachycardia
normal sinus rhythm with faster than 100bpm
Atrial Flutter
atria beat regularly, but faster than normal and more often than the ventricles do. Can be a ratio of 4/1
Atrial Fibrillation
atria beat irregularly. The SA node is firing so fast that the AV node cannot keep up with the signals. Classic rhythm strip with NOT have a P wave because the SA node is firing really fast
Asystole
no beats. Can be treated with medications.
ROSC
Return of Systemic Circulation
Heart Block:
Signal between atria and ventricles message pathway is interrupted. This is a medical emergency. Can be partial or total
Sinus Bradycardia:
heart beat in a normal sinus rhythm, however, it is under 59 bpm
Prior goal of pharmacotherapy
suppress dysrhythmias resulted in higher mortality rate among patients receiving antidysrhythmic drug therapy than those who were not
Antidysrhythmic drugs can
worsen existing dysrhythmias, may cause new dysrhythmias
Newest goal of therapy
prevent, relieve symptoms and prolong survival
Cardioversion
nonpharmacologic strategy: stopping the heart with a shock hoping that the heart beat will come back normal
Defibrillation
nonpharmacologic strategy: Vtac and Vfib are shockable by defib.
Radiofrequency Catheter Ablation
nonpharmacologic strategy: procedure where the doctor uses a cath to send radiofrequency energy to make circular scars around the heart and cells that are causing the dysrhythmias to burn out the areas and stop those cells from firing.
Pacemakers
utilized for sinus bradycardia. Or bradyarrhythmias for people whose heart rate goes below 40. This gives the heart a little shock that forces the heart to beat when it senses the dropped heart rate.
Atrial Fibrillation
if the ventricles are contracting too much, blood might be stored in the atria and then stored blood might clot. When that portion of blood gets into the ventricles and then they get into the lungs.
***Must be on some type of blood thinner
Sodium Channel Blockers
atrial dysrhythmia, Supraventricular Tachycardia (bursts of high rapid heart rates).
MOA depends on the class (IA, IB, IC) the medication is in
Sodium Channel Blockers SE
arrhythmias, Bradycardia, hypotension, respiratory Depression, dizziness, syncope, drowsiness, fatigue, confusion, anticholinergic
Sodium Channel Blockers EX
quinidine, lidocaine
Concerns: interfere with anticoagulants (which all atrial fib patients are on) and…obviously not good for someone with respiratory issues
Beta Adrenergic Blockers
Reduce activation of beta receptors=decrease conduction through SA/A node=decrease automaticity=slow HR
Beta Adrenergic Blockers Effect
Decreases cardiac excitability, cardiac workload, and oxygen consumption
Kinda like a slap to the face
Beta Adrenergic Blockers TX
management of dysrhythmia from excessive SNS stimulation, a-fibrillation, & a-flutter (thought to slow the ventricular rate), post MI/CHF (thought to prevent v-fibrillation)
Nursing Concerns for BAB
use with Verapamil (Ca+ blocker) can increase RF HB and bradycardia and hypotension
Potassium
Main intracellular ion/involved with cardiac rhythm (contractility of the myocardium/heart muscle)
Normal value: 3.5-5.0 mEq/L
Hypokalemia
less than 3.5. Sx: ventricular dysrhythmias, muscle weakness, decreased DTRs, weak peripheral pulses
TX for more K
Increase dietary K+ rich foods
Oral (preferred): no more than 20 mEq/L/hr. Give with meals/assess swallowing. Pills can be scored.
20 mEq po every two hours because it can only be absorbed 20/hour
Peripheral IV: 20-40 mEq/L; do not exceed 20 mEq/hr: if burning occurs, stop and assess the site (mix this in a liquid!)
Hyperkalemia
greater than 5.0 mEq/L. Sx: dysrhythmias, V-fib, HB, cardiac arrest, muscle twitching, numbness in hands, feet, and mouth
TX of Hyperkalemia
Restrict dietary K+ rich foods
Sodium polystyrene (Kayexalate): binds K+ and causes diarrhea
IV administration of insulin/dextrose shifts K+ back into cells and lowers the serum potassium
Common with end stage renal failure
Potassium Channel Blockers
inhibits adrenergic stimulation:
Block potassium channels=prolongs duration of action potential=slow repolarization=prolong refractory period
Potassium Channel Blockers TX
IV for life threatening tachy-dysrhythmias (not first line r/t RF pulmonary toxicity)
PO for recurrent tachycardia, V & A fibrillation and A-Flutter
Potassium Channel Blockers SE
Bradycardia, hypotension, worsen or new dysrhythmia, pulmonary toxicity (pleuritic pain, lung sounds fever, change in respiratory pattern). Don’t like to use it for respiratory pts. (IV), hepatotoxicity (drinker), blurred vision/photosensitivity
ALT/AST: Liver function tests to check before administering this medication
K+ Channel Blockers Medications
amiodarone (IV in emergencies or PO), dofetilide (Tikosyn given IV over night for people. Risk of QT wave prolongation which shows us that the ventricles are not contracting at a fast enough rate for the system to sustain) ibutilide, sotalol
Calcium Channel Blockers Function
Block calcium ion channels=reduce automaticity in SA node and slow the conduction through AV node=slow HR=prolong refractory period.
**Avoid Grapefruit Juice
Calcium Channel Blockers TX
supraventricular dysrhythmias (A-fib, SVT, atrial flutter) (@SA&AV nodes) tachycardia
*Can be an emergency medication for A-fib, SVT requiring IV administration
Calcium Channel Blockers SE
Bradycardia, hypotension, (HA, dizziness, lightheadedness), flushed skin, MI, hepatotoxicity, PERIPHERAL EDEMA
***Caution with HB, sick sinus, HF, hypotension, Hepatic/renal insufficiency, pregnancy
diltiazem, verapamil
Ca+ Channel Blocker Medications
Adenosine
Used for SVT when a vagal maneuver does not work
Given as a rapid bolus because the high metabolism
Depresses the conduction @ AV node=restore NSR in SVT patients
Naturally occurring component of all body cells
vagal maneuver
action to take when you need to stop an abnormally fast heart rate. Tell the patient to hold their breath and bear down for 20 seconds. Sticking your face in a bowl of icewater might work too.
Atherosclerosis
sometimes called hardening or clogging of the arteries, is a buildup of cholesterol and fatty deposits called plaques on the inner walls of the arteries
Coronary Heart Disease
Is the narrowing or blockage of the coronary arteries, usually caused by atherosclerosis.
Chronic Coronary Artery Disease leads up to it
Angina
Clinical Manifestation of Myocardial Ischemia
Stable Angina
classic, typical, exertional angina (Stable will go away after like 5 minutes)
Results when myocardial O2 demand is greater than the O2 supply to the heart muscle
Often results from exercise, physical activity, elemental exposure to cold, emotions/stress
TX for Stable Angina
thrombolytics (Lyce the clot) and interventional therapies (stents)
Variant Angina
occurs at rest/minimal exertion, HS (at bedtime), same time of day, cyclic 3-6 mos, subsides
Acute Coronary Syndrome (ACS)
Unstable Angina: ie: crescendo, rest or preinfarction angina
Acute pain occurs @ rest and lasts longer than 20 minutes
** can occur hours/days prior to acute myocardial infarction
** ACTION=IMperative! Time=Tissue
2 Types of Myocardial Infarctions:
NSTEMI, STEMI
NSTEMI
non-ST elevate Myocardial infarction. Interval between depolarization and polarization is there and not very much changed
STEMI
greater than 20 minutes persistent ST elevation on EKG (Very dangerous)
Cardiac Isoenzyme
Indicates damage to skeletal, visceral, or cardiac muscle. We would conclude cardiac
Cardiac Troponin 1 and Troponin T
biomarker of myocyte injury
Non-Pharmacologic Management of CAD
Cardiac Cath, coronary artery bypass graft (find a venule/artery that they cannot reopen so they cut out that artery that is bad and reconnect it to another artery), intracoronary stent
Nitrates
Potent Vasodilators
Relax and dilate veins, arteries, and capillaries; increase blood flow; lower systolic pressure
Relief of and prevention of angina pain
Decreases preload and afterload
Nitroglycerin Isosorbide dinitrate + Isosorbide mononitrate
Nitrates Examples
Nitrates SE
Severe headache, dizziness, bradycardia, syncope, hypotension RT: hemodynamic changes responsible for preload reduction and vasodilation
Nitrates Administration
Typically taken sublingual to prevent first pass effect in three doses: take one, 5 min, if pain stays, take 2 and wait 5 min, and make sure that you are going to the phone to call 911 if you need a third dose
Needs to be a brown bottle because it is degridated/light sensitive
Can be PO or translingual spray, or IV, or as a patch
Half life, 1-4 minutes. Rapidly absorbed
Beta Adrenergic Blockers + CAD
decrease cardiac workload by slowing the heart rate which decreases blood pressure and reduces contractility which INCREASES the O2 to the heart.
Cornerstone daily medication for patients with angina.
Calcium Channel Blockers + CAD
inhibits the influx of calcium entering through the slow channels which produces vasodilation of the peripheral blood vessels and coronary arteries. It does not affect the HR. Used for bradycardia. First pass metabolism is in the liver and it is fecal and urinary excretion
Nifedipine
Dose related, Ca+ channel blocker, Grapefruit juice will increase the effect, this medication will increases serum digoxin levels, cannot be used with adrenergic stimulants
Ranolazine
anti-ischemic metabolic modulator=first line treatment for chronic angina
atorvastatin, cholestyramine, and niacin
Dyslipidemic drugs: management of patients with major risk factors for atherosclerosis and vascular disorders (CAD, stroke, and peripheral arterial insufficiency) when lifestyle changes alone do not reduce blood lipids
Aspirin
antiplatelet effect with at lower doses effectively suppress platelet aggregation w/o without affecting important endothelial cell function. 81mg of Aspirin. Aspirin is the standard
Glycoprotein (GP)
IIb/IIIa receptor antagonists inhibit platelet aggregation for post MI
Post MI antiplatlets
The purpose of giving thrombolytic agents following a STEMI is to dissolve thrombi and reestablish blood flow as quickly as possible, prevent or limit tissue damage, and maximize functional improvement. The antiplatelets are daily medication for prevention.
Adenosine diphosphate (ADP)
receptor antagonists have antiplatelet effects similar to aspirin.
Morphine
opioid analgesic: pain/anxiety decrease preload. Primary reliever of pain management in post MI in patients with unacceptable levels of pain
hypotension
Systolic pressure less than 90. This means that there is decreased perfusion, decreased blood flow, and decreased oxygen to the tissues in order for the tissues to survive
Chronotropic effect
Change in HR
Dromotropic effect
causing a change in speed of electrical conduction in the heart
Inotropic effect
causing a change in the myocardial contraction
Normotrophic Effect
Having normal blood pressure
Pressor
effect that increases blood pressure
Shock
clinical condition initiated by compromised oxygen delivery, oxygen consumption, and/or oxygen utilization that leads to cellular death or tissue hypoxia
Acute hypotension is a sign of
Shock. Circulatory failure=hypotension=decrease in tissue perfusion
Hypovolemic Shock
when there is not enough circulating volume. Low blood volume. This can be the result of trauma, hemorrhage, burns, diabetic insipidus and diabetic ketoacidosis. Children can get this from vomiting and diarrhea
Cardiogenic Shock
pumping problem with the heart that can occur from an MI, dysrhythmia, or an improper valve closure problem between ventricle and atrium
Obstructive Shock
when there is a mass (tumor) or accumulation of fluid in an area or a blood clot. Causes heart to not pump
Disruptive Shock
when there is a state of massive vasodilation. For some reason the vessels get really big.
Anaphylactic Shock
Type of Disruptive Shock. major vasodilation from a histamine release in a severe allergic reaction
Neurogenic Shock
Type of Disruptive Shock when there is major vasodilation from high level spinal cord injury because there is a loss of signals for the sympathetic system. Message not sent to constrict
Septic Shock
Type of Disruptive Shock major dilation release of inflammatory mediators as a result of an overwhelming infection. Tx: IV fluids and antibiotics
Three stages of Shock
Compensative Phase
Uncompensated/Decompensated
Final “End Stage” Phase
Compensative Phase of Shock
Preshock. When the body starts to sense that there is a low fluid volume it attempts to restore itself and return to homeostasis. When the heart senses that the blood volume is low it is gonna try to beat faster so that the body gets the blood that it needs. Can also compensate through vasoconstriction (SNS)
Uncompensated/Decompensated Phase of Shock
r/t the compensation is not able to do the job and the shock is left untreated or undiagnosed. Typically because there is not enough blood to work with. This leads to organ dysfunction. WE are gonna see cardiac output, hypoperfusion, endothelial damage, microvascular thrombosis. Decreased capillary blood flow. WE heart rate will decrease. Patients will be clammy, cool, sweaty, restless, and decrease in urine output. Metabolic acidosis.
Final “End Stage” Phase of Shock
Irreversible: Permanent tissue or organ damage. They are having multiple organ failure. Renal failure is the first to go. No urine production whatsoever. The patient is in lactic acidosis (buildup of acid causes an imbalance in pH. Not enough oxygen to break down glucose and glycogen)
Therapy for Hypotension/Shock:
Adrenergic Agonist: Vasopressors
Epinephrine (Adrenaline)
Dopamine: Potent alpha adrenergic agonist
Dobutamine
Adrenergic Agonist
cause potent peripheral arterial vasoconstriction, which will cause an increase in blood pressure and at times will also increase the heart rate, it will also increase the force of contraction and cardiac output
Adrenergic Agonist Contraindications
cardiac dysrhythmias, angina pectoris, hypertension, hyperthyroidism, and cerebrovascular disease, narrow angle glaucoma. Toxic to the tissues. This medication has to be administered in a central line so that the medication goes right into the bloodstream
Norepi, phenylephrine, epinephrine, dopamine
Adrenergic Agonists
Epinephrine (Adrenaline)
stimulates beta and alpha adrenergic receptors: potent vasoconstrictor. Emergency medication that increases HR and constriction
Dopamine
Potent alpha adrenergic agonist
Low dose: renal and coronary arteries
High dose: increase heart rate and vasoconstrictor (for shock)
Dobutamine
Stimulates Beta 1 receptors
Low dose: increase contractility and increase cardiac output
Does not cause tachycardia
***incompatible with BICARB which is typically utilized as a buffer when we have lactic acidosis
Phentolamine
alpha blocker that you use when leaking alpha adrenergic medication causes necrosis.
Cardiomyopathy
disorder of the heart muscle where it becomes weak
CHF
Complex clinical condition where the heart cannot pump enough blood to meet bodies O2 and nutritional needs
Goal for CHF Patients
symptoms management. Decrease fluid management so that the heart can pump more efficiently
Causes that impair pumping ability of the heart
hyperthyroidism (thermoregulator). Excessive fluids/blood transfusion. When blood is thicker it makes the heart work harder. Fluid volume overload. Antidysrhythmic medications. Water retention.
Endothelial Dysfunction
narrowing of vessel lumen which increases pressure. Leads to clot formation. Leads to vasoconstriction
Systolic Heart Failure
Failure of ventricle contraction. Most common. Reduced EF
Diastolic Heart Failure
Failure of Filling: Stiff noncompliant muscle. Normal EF
Right Sided Heart Failure sx
Weight gain, JVD, Peripheral Edema, Fatigue
Ascites (swelling around abdomen), Enlarged liver and spleen, Lack of appetite, Weight gain
Core pulmonale
enlargement and failure of the right ventricle of the heart as a response to increased vascular resistance.
Left-Sided Heart Failure sx
Right ventricle is pumping really hard against narrow blood vessels. SOB
Crackles, Activity intolerance, Dizziness, Because the blood is backing up from the left side of the heart and it is staying in the lungs, Tacipnea: rapid breathing. Confused: Orthopnea
Digoxin
Management of mild-moderate heart failure. Positive inotropic effect. Management of atrial fibrillation: negative chronotropic effect which SLOWs the heart. Allows more Ca+ to enter the cells which increases intracellular Ca+ which decreases the workload of the heart
Digoxin Adverse Effects
weakness, HA, Drowsiness, vision changes, GI upset/anorexia, Arrhythmias, breast enlargements
Monitor for improving signs of HF/Afib and monitor for DIG TOXICITY. HOLD if serum level is greater than 2nm/mL
Therapeutic Normal dig levels
0.8-2nm/mL
Contraindications for Digoxin
PMHx of V tach/V fib, HB/Sick sinus, Acute MI, Renal insufficiency, Electrolyte abnormalitie
Signs of digoxin toxicity:
Yellow/green vision blurring
Ventricular rhythm changes
Abdominal discomfort
Premature ventricular contractions
Which blood results can cause dig toxicity even when the dig levels are WNL
hypokalemia, hypomagnesemia, and hypercalcemia
digoxin antidote
digoxin immune Fab
Phosphodiesterase Inhibitor
Long term bridge therapy (combines the heart) in heart failure, Increase Ca++ in cell.
Increase the force contraction in the ventricle, positive inotropic effect, relaxation in the vascular smooth muscle, systemic and pulmonary dilation, decrease in preload and afterload so the tired heart does not have to pump so hard against preload and afterload
milrinone
Phosphodiesterase Inhibitor
milrinone SE
Thrombocytopedia, burning at injection site, anorexia, N/V, cp
Human B Type Naturinic Peptides
Hormones that help maintain sodium and fluid balance which reduces preload and afterload
Human B Type Naturinic Peptides Action
release increases sodium excretion by the kidney and diuresis, direct vasodilation, increased glomerular filtration rate. Gonna help the kidneys to release the sodium. Not great for someone with kidney or renal disease
Nestride
Human B Type Naturinic Peptides Action
Adverse Effects of Nestride
hypotension, HA, N/V, backpain, dizziness, ventricular tachycardia, anxiety, insomnia, bradycardia
Monitor BP and urine output and BMP for sodium
Sacubitril/valsartin
Management of chronic heart failure in patients with reduced ejection fraction
Sacubitril/valsartin Therapeutic Action
Sacubitril inhibits the enzyme neprilysin, responsible for degradation of atrial and brain natriuretic peptide (BNP), the peptides responsible for lowering blood pressure and blood volume along with Valsartin (ARB)
Contraindication Sacubitril/valsartin
Lithium, pregnancy, must be on birth control
Sacubitril/valsartin AE
hypotension, hyperkalemia, cough, renal impairment, dizziness, angioedema may also occur
Sinoatrial node modulators
Selective inhibition in the SA node=decreased firing from the SA node=decreased heart rate=allows more ventricular filling. Reduce risks in worsening heart failure for patients who have chronic heart failure while they are in the hospital
Ivabradine
Sinoatrial node modulators
Ivabradine SE
Bradycardia, hypotension, and fibrillation, and phosphine (a ring or spot of light caused by pressure on the eye orbital)
Contraindications for Ivabradine
acute, decompensated heart failure, bradycardia, hypotension, heart blocks, sick sinus syndrome, pacemaker patients, severe hepatic impairment, grapefruit juice
diarrhetic + Heart Failure
Pt. will almost always be on a diarrhetic.
If we see a 4lb increase in body weight we need to see them. Sodium and water stick to the body!
Diuretics nighttime dose is always at around 5pm
PO first, IV second,
Spironolactone
K+ sparing diuretic
lipoproteins
Each lipoprotein contains cholesterol, phospholipids, and triglyceride bound to protein
cluster of conditions that occur together that end up increasing the risk of heart disease, stroke, and type II diabetes.
High waist circumference
High triglyceride levels resulting from high carbs and dietary proteins
High LDL (low density lipoprotein)
Low HDL (High density lipoprotein)
High blood pressure
High fasting glucose
hypertension
Dyslipidemia
AKA hyperlipidemia: increase levels of lipids in the blood
Major risk factor for CAD
Associated with atherosclerosis
s/sx associated with dyslipidemia
MI
Ischemia
CVA
Peripheral arterial occlusive disease
Primary Dyslipidemia
genetic/familial
Mutation in the LDL receptor and they have an increase in their LDL lifelong
1/500 people
Secondary Dyslipidemia
habit/lifestyle
Alcoholism, DM, hypothyroidism
Obesity. Obstructive liver disease
HIgh cholesterol Symptoms
Loose stools
Poor appetite
Fatigue
Depression
Weight gain
Bumps around their eyes
Stomach distension
Heart pain
Aching pain
National Cholesterol Education Program III Treatment Guidelines
Total Serum Cholesterol (less than 200)
LDL (less than 100)
HDL (between 40-60, and greater than 60 is good)
Treatment according to total and LDL cholesterol because these risk for cardiovascular disease
Assessment and Treatment plan for HIgh cholesterol
- Determine hypoprotein level after 9-12 hour fast
- Identification of presence of atherosclerotic disease that confers high risk for coronary heart disease events
- Determine other risk factors besides a high LDL
LDL
low density lipoprotein. BAD
HDL
High density lipoprotein
Characteristics of Antidyslipidemics
Decrease blood lipids
prevent /delay atherosclerosis plaque development
Promote regression of existing atherosclerotic plaque.
Reduce morbidity and mortality from cardiovascular disease
hydroxymethylglutaryl-coenzyme A reductase inhibitors
Decrease cholesterol production=decreases total cholesterol, LDL, VLDL and triglycerides without reducing HDL
Atorvastatin, pradistatin, Rosuvastatin, Simvastatin
hydroxymethylglutaryl-coenzyme A reductase inhibitors examples
Pharmacokinetics of hydroxymethylglutaryl-coenzyme A reductase inhibitors
extensive first pass effect (liver)/food decreases absorption rate/80-85% excreted in stool, the rest excreted in the urine
hydroxymethylglutaryl-coenzyme A reductase inhibitors Side Effects
MYALGIAS (dysfunction in the muscle fibers), leg pain, nuasa, constipation, diarrhea
hydroxymethylglutaryl-coenzyme A reductase inhibitors
Drug Interactions
MG+ antacids, “azole” antifungals, some antibiotics, cholestyramine
hydroxymethylglutaryl-coenzyme A reductase inhibitors Considerations
Evening or HS administration (2100) medication r/t cholesterol synthesis occurs at this time of day
Avoid grapefruit juice, vitamin B, pomegranate juice
Monitor liver function tests because it has a big first pass effect
Watch for rhabdomyolysis (severe muscle cramps, cola colored urine, extreme fatigue) stop med and call doctor.
BLACK BOX: X CATEGORY
Bile Acid Sequestrants
Binds bile acids in the intestinal lumen = bile acids excreted via stool= prevents recirculation to liver = stimulates increase bile acid synthesis from cholesterol in liver = increases cholesterol to liver = lowers serum LDL
Cholestyramine
Bile Acid Sequestrant example
Cholestyramine Pharmacokinetics
not absorbed with oral administration. Excreted unchanged in stool/decrease LD within a week of use and max level will maximize in 1 month
cholestyramine SE
GI fullness, flatulence, constipation, diarrhea
Cholestyramine Considerations
It stops absorption of (DIG, glipizide, folic acid, propranolol, thyroid hormone, thiazide diuretics, warfarin)
Fibrates
increase oxidation of fatty acids in the liver and muscle tissue. Decrease hepatic production of triglycerides, VLDL, and increase HDL
Fenofibrate + gemfibrozil
Fibrates Examples
Fibrates Pharmacokinetics
oral administration/highly protein bound, peak 6-8 hours, liver metabolism, urinary excretion
Fenofibrate + gemfibrozil Side effects
RF gallstones: not for pts. With existing or preexisting gallbladder disease
Nursing Concerns for Fenofibrate
can enhance the effects of warfarin, increase RF myopathies or rhabdomyolysis with STATINS
gemfibrozil
must be taken on an empty stomach
Cholesterol Absorption inhibitors
Inhibit absorption of cholesterol in the small intestines & decreases delivery of intestinal cholesterol to the liver = reduced hepatic cholesterol stores , increasing cholesterol clearance from the blood
Ezetimibe
Cholesterol Absorption inhibitor
Ezetimibe: Pharmacokineteics
protein bound, metabolized in small intestine and liver and excreted in stool. Peak effect after in4-12 hours.
Ezetimibe Consideration
Category C
PCSK9 Inhibitors
antibody that inactivates protein in the liver that regulates lifespan of cholesterol, promoting modulation of the receptors=prolong receptor activity=promoting clearance of cholesterol=can have a 60-70% reduction in LDL
Alirocumab
PCSK9 Inhibitor
Alirocumab Consideration
Used for patients with PRIMARY hyperlipidemia when their statin dose is maxed out
subQ every 2-4 weeks/doses vary. 3-7 day max serum concentrations
Niacin (Vitamin B3)
boosts levels of healthy HDL levels and lowers triglycerides and modestly lowers LDL
Niacin (Vitamin B3) SE
facial flushing, stomach upset, diarrhea, can raise blood sugar (not good for DM)
Omega 3 Fatty Acids
Dyslipidemic
Advicor
extended release niacin and lovestatin combination medication
Simcor
simvastatin and niacin combination therapy
Hematopoietic Disorder
diseases that cause the blood to change. Not enough, too much, RBC cells too large, viscosity of the blood, hemoglobin levels
Hematopoiesis
the process of making blood that happens in the bone marrow
stem cells
grow into all three types of blood cells (red, white, platelets). They make copies of themselves and produce mature blood cells and then leave the blood marrow.
Hematopoietic Growth Factor
determines survival and proliferation of hematopoietic lineage and can transduce a genuine lineage determining signal in hematopoiesis and initiate the cell maturation process
Hematopoietic Cytokines
Extracellular ligands that stimulate hematopoietic cells to differentiate into eight principle types of blood cells (white blood cells)
Regulate many cellular activities
Act as chemical messengers among cells
Act as growth factors for blood cells
Perform by binding to receptor on target cells
Interleukins
Affect immunogenic cell response. They are either Stimulator or Suppressive
Erythropoietin
Hormone secreted by kidneys which stimulates RBC differentiation, Maturation, and proliferation. Stimulates bone marrow to produce RBC (transport vehicles)
Conditions that will trigger this are hemorrhage, anemia, COPD, and high altitude
Higher red blood cells means higher ability for blood to carry oxygen to the cells
Immune System
Immune system cells identify and remove injured, damaged, dead or malignant cells.
Leukocytes
(fighters) that circulate in blood and lymphatic vessels or reside in lymphoid tissues. Make up
CBC w/ Differential
gives a count of each type of white blood cells. Helps a doctor know exactly WHY a WBC is up
Leukocytosis
increase in WBC
Leukopenia
Decrease in WBC
Anemia
a lack of RBC or disfunctional RBC in the body which leads to reduction of Oxygen flow to body’s organ because the RBC houses hemoglobin which carry the oxygen to the tissue.
Iron Anemia
decrease of Iron in the blood which leads to a decrease in RBC count. Can be because of store depletions.
At Risk: Menstruating women, lactating women, rapidly growing kids, losing blood at large volume through a GI bleed
Pernicious Anemia
deficiency of Vitamin B12: tx: IMb12 injections or B12 oral supplements
Megaloblastic Anemia
a person has larger than normal blood cells due to inhibition of DNA synthesis during RBC production. Cell cycle cannot migrate from G2 to the mitosis phase so the cells get bigger and bigger without division
Megaloblastic Anemia S/Sx
glossy red tongue and diarrhea.
Results from a deficiency of Vitamin B12 and folate.
Sickle Cell Anemia
Sickle cells do not allow the O2 to attach which limits perfusion.
Hydroxyurea/antimetabolite:
helps prevent formation of “sickle” shaped cells
Immunostimulants
drugs that stimulate/enhance the immune system by inducing activation of increasing any of its components
Used to restore normal function or increase the ability of the immune system to eliminate harmful invaders
Typically these are injected
Epoetin alpha
darbepoetin
Induces Erythropoiesis leading to an increase in Hgl and Hct levels
Treatment of anemia in renal failure, AIDS, and cancer
Stimulates the patient’s own body to avoid blood transfusion.
Epoetin alpha/darbepoetin Administration
IV/SQ. Metabolized in serum/excreted in urine. injectable with an airlock. Monitor CBC for INCREASE in RBC, Hgb, Hct, increase energy and exercise tolerance
Epoetin alpha/darbepoetin Considerations
uncontrolled hypertension (we don’t wanna make the blood even thicker!)/allergy/normal renal function (kidneys are producing enough on its own)
Granulocyte Colony Stimulating Factors
Stimulate blood cell production in bone marrow for patients with neutropenia (chemotherapy induced febrile neutropenia, acute myeloid leukemia, cancer patients receiving bone marrow transplants, or chronic idiopathic neutropenia)
Filgrastim
stimulates neutrophil progenitor cell proliferation and differentiation in bone marrow=increase number of mature neutrophils
Filgrastim Considerations
SQ/IV. Completely absorbed over four days
flu like symptoms, fatigue, bone pain, thrombocytopenia (bleeding gums/ease of bruising)
Ferrous aspartate
Ferrous gluconate
ferrous sulfate
iron dextran
regain positive iron balance, treatment of iron deficient anemia
IV, PO
Z-track for IM-iron dextran
Iron is Absorbed in small intestine
ferrous sulfate Adverse Effects
GI effects: constipation
Administer between meals if possible (increase absorption)
Vitamin C given with iron can increase absorption
If oral liquid, use straw because it stains the teeth
Plasminogen and Fibrin
used to form the clot which stops the blood flow and keeps the blood vessel repaired.
Plasmin
dissolves the clot once it is all healed
Liver
primary organ responsible for clotting factors
Intrinsic Pathway
trauma INSIDE the blood vessel itself. OR blood is exposed to collagen factor 12
Extrinsic Pathway
vascular tissue trauma
Thrombogenesis
Formation and dissolving of thrombi
Normal Body Defense
Arterial Thrombosis
obstruct arterial blood flow
Venous Thrombosis
result of venous stasis
Less cohesive than arterial thrombus and travel quickly and detach more easily
MORE severe than arterial thrombosis
Prophylactic DVT prevention
Heparin subque
Atherosclerosis
Elevated serum lipid levels
Lipid Filled macrophages
Fibrous Plaques and lesions
Severe ulceration and scarring tissue
Antithrombotic + Antithrombolitic
Anticoagulants
Antiplatelets (platelet life: 7-10 days)
Thrombolytics
Anticoagulants
DO NOT dissolve formed clots
Prevent formation of new clots
management of thromboembolic disorders
Thrombophlebitis
vein inflammation usually occurs by irritation to a venus venule by a clot
Heparin
Given to prevent new clot formation and extension of clots present
IV: monitor aPTT/PTT
Test and normal range for heparin
aPTT/PTT: 60-80
SQ: prophylaxis for DVT formation prevention in bed restricted hospital patients (dose 5000u/mL)
Heparin Antidote
protamine sulfate (basic)
Warfarin Test and Result
PT/INR: 2-3
Antidote for Warfarin
Vitamin K+
Considerations for Warfarin
avoid foods high in vitamin K
Avoid grapefruit juice, cranberry juice, and alcohol (enhance the effect)
Kale, broccoli, soybean oils
Fondaparinux
Factor Xa Inhibitor
SQ injection only
Extremely expensive ($3726/10 doses)
Prefilled
Dabigatran
Direct thrombin inhibitor
Tx: afib and stroke prevention
PO bid
Dabigatran Antidote
Idarucizumab
Rivaroxaban
Factor Xa Inhibitor
Tx of afib, stroke prevention, secondary DVT (DVT came from a known cause) prevention
PO once a day
Apixaban
Factor Xa inhibitor
Tx of afib, stroke prevention,
Given bid
BLACK BOX for Xa Inhibitors
don’t stop abruptly due to rebound thrombotic event
Ecchymosis
Excessive bruising
Subdural hematoma
Bleed in the brain
Hemoptisis
Bloody sputum
Antiplatelets
Inhibit platelet activation
Inhibit platelet adhesion
Inhibit platelet aggregation
Inhibit procoagulant acuity
Clopidogrel
Antiplatelet
Irreversibly inhibit ADP receptors on the surface of platelets. No antidote
Extensive first pass effect. Onset of action is slow so a loading dose is necessary
Can be used in conjunction with aspirin
Significant individual variability in response
Most common SE=pruritus (itching), rash, purpura, diarrhea
Thromboxane A2 Inhibitors
Antiplatelet
Inhibits the synthesis of prostaglandins=prevents formation of thromboxane A2=prevents platelet aggregation
81mg Aspirin
Thromboxane A2 Inhibitor
Abciximab
monoclonal antibodies that prevent the binding of fibrinogen, this action will inhibit platelet aggregation.
Used for interventional procedures with ASA and Heparin
Cilostazol
inhibits platelet aggregation and produces vasodilation
Used for intermittent claudication
Anagrelide
inhibit platelet aggregation induced by cAMP phosphodiesterase
Reduce platelet counts R/T essential thrombocythemia
intermittent claudication
Pain with activity caused by reduced blood flow to a limb. Symptom of PVD
Thrombolytic Agents
given to dissolve thrombi and stimulate conversion of plasminogen to plasmin (breaks down thrombin)
Alteplase
High Risk Emergency medication that thins blood and gets out of the blood in 10 minutes. This is used for stroke or blood clots
Headache and hypotension indicate that the patient is bleeding internally and this is BAD when taking this medication.
